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Mitochondrial damage and iron accumulation from hepatitis C virus are linked to the development of hepatocellular carcinoma (HCC), according to an extensive literature review.

E.H. Cook, Jr./CDC

Although the mechanisms underlying the hepatocellular carcinoma development are not fully understood, it is known that oxidative stress exists to a greater degree in hepatitis C virus (HCV) infection, compared with other inflammatory liver diseases. Such stress has been proposed as a major mechanism of liver injury in patients with chronic HCV, the authors reported in Free Radical Biology and Medicine.

Patients with HCV have significant hepatocellular mitochondrial alterations, and iron accumulation is also a well-known characteristic in patients with chronic HCV. Such alterations in mitochondria and iron accumulation are closely related to oxidative stress, since the mitochondria are the main site of reactive oxygen species generation, and iron produces hydroxy radicals via the Fenton reaction, according to the review.

“The greatest concern is whether mitochondrial damage and iron metabolic dysregulation persist even after HCV eradication and to what extent such pathological conditions affect the development of HCC. Determining the molecular signaling that underlies the mitophagy induced by iron depletion is another topic of interest and is expected to lead to potential therapeutic approaches for multiple diseases,” the researchers concluded.

Support was from the Research Program on Hepatitis from the Japan Agency for Medical Research and Development. The authors reported no disclosures.

SOURCE: Keisuke H et al. Free Radic Biol Med. 2019;133:193-9.

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Mitochondrial damage and iron accumulation from hepatitis C virus are linked to the development of hepatocellular carcinoma (HCC), according to an extensive literature review.

E.H. Cook, Jr./CDC

Although the mechanisms underlying the hepatocellular carcinoma development are not fully understood, it is known that oxidative stress exists to a greater degree in hepatitis C virus (HCV) infection, compared with other inflammatory liver diseases. Such stress has been proposed as a major mechanism of liver injury in patients with chronic HCV, the authors reported in Free Radical Biology and Medicine.

Patients with HCV have significant hepatocellular mitochondrial alterations, and iron accumulation is also a well-known characteristic in patients with chronic HCV. Such alterations in mitochondria and iron accumulation are closely related to oxidative stress, since the mitochondria are the main site of reactive oxygen species generation, and iron produces hydroxy radicals via the Fenton reaction, according to the review.

“The greatest concern is whether mitochondrial damage and iron metabolic dysregulation persist even after HCV eradication and to what extent such pathological conditions affect the development of HCC. Determining the molecular signaling that underlies the mitophagy induced by iron depletion is another topic of interest and is expected to lead to potential therapeutic approaches for multiple diseases,” the researchers concluded.

Support was from the Research Program on Hepatitis from the Japan Agency for Medical Research and Development. The authors reported no disclosures.

SOURCE: Keisuke H et al. Free Radic Biol Med. 2019;133:193-9.

 

Mitochondrial damage and iron accumulation from hepatitis C virus are linked to the development of hepatocellular carcinoma (HCC), according to an extensive literature review.

E.H. Cook, Jr./CDC

Although the mechanisms underlying the hepatocellular carcinoma development are not fully understood, it is known that oxidative stress exists to a greater degree in hepatitis C virus (HCV) infection, compared with other inflammatory liver diseases. Such stress has been proposed as a major mechanism of liver injury in patients with chronic HCV, the authors reported in Free Radical Biology and Medicine.

Patients with HCV have significant hepatocellular mitochondrial alterations, and iron accumulation is also a well-known characteristic in patients with chronic HCV. Such alterations in mitochondria and iron accumulation are closely related to oxidative stress, since the mitochondria are the main site of reactive oxygen species generation, and iron produces hydroxy radicals via the Fenton reaction, according to the review.

“The greatest concern is whether mitochondrial damage and iron metabolic dysregulation persist even after HCV eradication and to what extent such pathological conditions affect the development of HCC. Determining the molecular signaling that underlies the mitophagy induced by iron depletion is another topic of interest and is expected to lead to potential therapeutic approaches for multiple diseases,” the researchers concluded.

Support was from the Research Program on Hepatitis from the Japan Agency for Medical Research and Development. The authors reported no disclosures.

SOURCE: Keisuke H et al. Free Radic Biol Med. 2019;133:193-9.

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